CD36 palmitoylation regulates the lipid metabolic homeostasis

Alterations in myocardial energy substrate metabolism following myocardial infarction (MI) results in structural and functional abnormalities of the heart. The fatty acid translocase CD36 (CD36), acrucial membrane protein, plays a pivotal role in regulating fatty acid (FA) uptake and lipid homeostasis. Here, we employed a comprehensive multi-omics analysis using a mouse MI model, integrating molecular biology, histological, transcriptomic and proteomic analyses. Our findings unveiled dysregulation in lipid metabolism, mitochondrial oxidative phosphorylation and related genes.